Hyperthermia aggravates status epilepticus-induced epileptogenesis and neuronal loss in immature rats.
作者： L. Suchomelova , M.L. Lopez-Meraz , J. Niquet , H. Kubova , C.G. Wasterlain
DOI: 10.1016/J.NEUROSCIENCE.2015.08.006
关键词: Anesthesia 、 Diazepam 、 Apoptosis 、 Endocrinology 、 Status epilepticus 、 Epileptogenesis 、 Hippocampus (mythology) 、 Hyperthermia 、 Pilocarpine 、 Internal medicine 、 Amygdala 、 Chemistry
摘要: This study tightly controlled seizure duration and severity during status epilepticus (SE) in postnatal day 10 (P10) rats, order to isolate hyperthermia as the main variable its consequences. Body temperature was maintained at 39 ± 1 °C hyperthermic SE rats (HT+SE) or 35 normothermic animals (NT+SE) 30 min of SE, which induced by lithium-pilocarpine (3 mEq/kg, 60 mg/kg) terminated diazepam cooling NT. All video/EEG measures were similar between HT+SE NT+SE pups. At 24h, neuronal injury present amygdala group only, far more severe hippocampus than Separate groups monitored four months later for spontaneous recurrent seizures (SRS). Only developed convulsive SRS. Both electrographic SRS (83% vs. 55%), but frequency higher (12.5 3.5 4.2 2.0 SRS/day). The density hilar neurons lower, thickness perirhinal cortex reduced, lateral ventricles enlarged over littermates HT/NT controls. In this model, greatly increased epileptogenicity neuropathological sequelae.
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